In the past few months, Europeans have heard some good news about climate change. In April, 2026, the European Commission launched a new €601 million LIFE funding programme to support climate adaptation, biodiversity, and clean energy projects across the region. Meanwhile, the German Government announced a €5 billion programme on May 5 to help industry reduce its carbon emissions. Some positive trends are also reported in the 2026 Europe report of the Lancet Countdown on health and climate change published in this issue, which measures 43 indicators, including seven new ones.
[Articles] The effects of the Rx Kids unconditional cash prescription programme during pregnancy and infancy on birth outcomes in the USA: a population-based, quasi-experimental study
With significant reductions in adverse birth outcomes, the treatment of perinatal poverty with a place-based intervention as replicable and scalable as Rx Kids has important implications for infants and society. These findings suggest that the economic hardship of the perinatal period, starting in utero, contributes to adverse outcomes and is addressable.
Self-Monitoring Risk Factors for Diabetic Foot Ulceration With the Feetchecker App: Mixed Methods Study
Background: A prevalent and serious complication of diabetes mellitus is the development of diabetic foot ulcer (DFU). There is a need for effective solutions that help prevent DFU to support our increasingly stressed health care systems. The use of mobile health (mHealth) tools has been shown to improve awareness and effective self-care management skills in people at risk of developing diabetic foot ulceration. Objective: In this study, we aimed to investigate the perceived usefulness, engagement, and overall user experience of the Feetchecker app, a self-monitoring mHealth app for people at risk of DFU. Methods: A total of 24 patients (mean age 71, SD 8.6 years) with type 2 diabetes mellitus at risk of developing diabetic foot ulceration completed a 3-month evaluation period (70 recruited, 36 included, 12 dropped out) of a self-monitoring mobile app called Feetchecker app. A mixed methods approach was used to combine insights from app data with qualitative data from a pre- and postsurvey as well as interviews with patients and involved podiatrists. Data were analyzed using descriptive statistics and thematic analysis. We evaluated overall use of the app, patient engagement, and user experiences. Results: Patients who fully completed the study conducted 393 feetchecks. In total, 7 patients sent in 9 pictures; all 7 were called for follow-up by a podiatrist. Overall, patients had a positive experience with the app and perceived the Feetchecker app as a valuable tool to monitor their feet for potential risk factors of DFU. Ease of use in performing a feetcheck and sending the podiatrist a picture was described as an important feature. Three main types of engagement with the Feetchecker app emerged: continuous, frequent, and no to little engagement. These patterns highlight enablers for self-monitoring such as ease-of-use, easy access to a podiatrist, and social support, as well as barriers such as digital skills and sustained engagement. Podiatrists highlighted the benefits of having patients report potential issues quicker and the ability to monitor their patients remotely. Challenges remain in integrating the promotion of the Feetchecker app into their consultations. Conclusions: The Feetchecker app supported patients in self-monitoring risk factors associated with DFU through routine checks and quick contact with a health care professional in case of a potential issue. Overall, patients described a positive user experience and considered the app helpful. While mHealth tools are not for everyone, user engagement for many patients was high and shows that such apps can offer support for people able to use them. Future research should focus on improving usability and engagement with the app as well as extend the way patients can communicate with health care professionals beyond a picture.
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Sea Cucumber Tissues Demonstrate Natural Immortality in Seawater
From the revived corpse of Frankenstein’s monster to the disembodied hand, “Thing,” in the Addams Family, reanimated tissue is one of the most enduring images in science fiction. The discovery of a sea floor-dwelling sea cucumber that scientists are calling a “real-life zombie” suggests that there may be some basis for that image in nature.
Scientists headed by a team at Memorial University of Newfoundland showed the continued viability of amputated tissue from the sea cucumber Psolus fabricii for more than three years in natural seawater. It’s the first known report of the long-term survival—and continued growth—of discarded tissue outside of a highly controlled, sterilized environment.
The discovery that these living P. fabricii explants (LiPfe) can survive for years in natural seawater without any supplementation challenges assumptions of what’s possible for tissue immortality and could have implications in areas including regenerative biology and tissue engineering. The findings could also lead to the development of experimental models for biological research that are more widely accessible, without the ethical and logistical challenges associated with many existing cell lines.
“We haven’t grown a new, complete sea cucumber yet, but we are seeing pretty stunning growth and diversification of cells literally years after this tissue was removed,” said research lead Rachel Sipler, PhD, a Bigelow Laboratory for Ocean Sciences senior research scientist. “It’s like a lizard that loses its tail. We know some lizards can grow new tails; we’re talking about whether the tail can grow a new lizard.”
Reporting on their findings in Science Advances (“Natural tissue immortality: Indefinite survival of sea cucumber explants,”) Sipler and colleagues stated, “Our findings challenge conventional perceptions of tissue immortality and present a new class of experimental model, free from ethical concerns, with substantial implications for regenerative biology, biomedical research, and tissue engineering.”
Over the last 200 years, scientists have tried to achieve cellular and tissular survival outside living hosts, “… but efforts have been met with limited success due to the highly degradable nature of tissue itself,” the authors wrote. Since the mid-20th century, scientists have made significant breakthroughs with immortal cell lines, such as HeLa cells, that can be grown in a lab and proliferate indefinitely for long-term research. In earlier studies, tissue cultures have only been maintained under axenic conditions that are tightly controlled, rigorously maintained, and lack any bacteria or other organisms. Even then, they have not demonstrated signs of actual healing and growth, nor retained the ability to move independently. “While immortal cell lines demonstrate indefinite proliferation in vitro, they lack structural integrity and complex tissue interactions,” the team continued. “Achieving this with complex, structured tissue represents the next step.”
Many echinoderms, including sea cucumbers, are known to display impressive regeneration capacity and negligible cell aging. “In the ongoing effort to understand tissue culture, regeneration, and immortality, researchers have naturally been drawn to echinoderms, a phylum with genetic and evolutionary links to vertebrates and examples of both extreme regenerative capacity and negligible cellular senescence,” the investigators noted. Lost tissue, though, was always assumed to eventually decay or die.
Yet, in what Sipler calls a product of “keen observation,” the researchers noticed that some discarded tissue from a tube foot of a sea cucumber hadn’t decayed after a number of weeks. In fact, it seemed to be growing. The researchers then ran a number of experiments in flowing seawater with tissue removed from the feet, main body, and tentacles of three individuals of P. fabricii, a cold-water species of sea cucumber.
They found evidence of diversifying cells, immune activity, and tissue reorganization in the explanted tissue. “In experimental trials, these explants, termed LiPfe (living immortal P. fabricii explants), displayed immune activity, cell cycling, tissue reorganization, and absorption of dissolved amino acids, underscoring their active living state,” they noted. And in the absence of a mouth, the cells appeared to be getting nutrients by absorbing amino acids dissolved in the seawater.
Even after three years, when the researchers stopped the experiments in order to publish, the tissue was still active. This ability to survive in a complex, stressful environment, Sipler said, makes this cell line unique compared to other tissue cultures. “Compared to other cells or tissues grown under laboratory setups that required strict parameters, including axenic conditions, LiPfe required nothing apart from natural running seawater,” they wrote. “Comparative experiments conducted on explanted tissues from related species demonstrated no equivalent tissue survival, highlighting the unique properties of P. fabricii, which do not have parallels in the current literature.”
“Natural seawater is just about the most microbially diverse, least clean approach we could take experimentally,” Sipler added. “Yet, that rich environment full of bacteria and all this organic matter was actually feeding them and allowing this tissue to heal and grow.”
The implications for biomedical sciences and engineering, the authors said, are profound, with potential applications in everything from tissue regrowth to anti-microbial healing. In their paper, the authors stated, “The discovery of LiPfe challenges the boundary between organismal life and cellular autonomy, compelling a redefinition of what it means for tissue to be alive.”
The discovery opens up new opportunities for biological research and education more broadly. The tissue they’ve preserved not only shows an unprecedented ability to maintain its structural integrity and complexity in culture. It can also be grown more easily in the lab and, as an invertebrate, isn’t subject to as many research restrictions, making it useful in contexts where there are legal obstacles or limited biosafety infrastructure for using human-based or other vertebrate cell lines.
As an oceanographer, Sipler noted that the exciting discovery drives home the incredible untapped potential of ocean life. “The best advances in science are made when you find a natural analog for what you’re studying,” she said. “Here is this species that has this groundbreaking ability, and we had no idea. It’s a reminder of how much is yet to be discovered in the marine environment, and how important it is to protect these resources that may hold really valuable knowledge for us.”
The post Sea Cucumber Tissues Demonstrate Natural Immortality in Seawater appeared first on GEN – Genetic Engineering and Biotechnology News.
Precision, Gene-Edited Antimicrobial Targets Difficult-to-Treat E. Coli
An oral, next-generation antimicrobial created using CRISPR-Cas gene editing could one day reduce the severity of a serious, food-borne infections that are generally untreatable with antibiotics.
The preclinical findings offer a potential new weapon in the armamentarium against Shiga toxin-producing Escherichia coli (STEC), a bacterium that causes nearly three million acute illnesses worldwide, mostly in children each year.
The precision gene therapy, called EB003, was able to significantly reduce the disease severity in an animal model of STEC infection.
“Although challenges such as dosing, resistance emergence, and delivery optimization remain, our findings provide a compelling foundation for the further development of EB003 and other CRISPR-based therapeutics,” reported Matthieu Galtier, PhD, of the Pasteur Institute in Paris, and co-workers in in Science Translational Medicine.
STEC is a notable public health threat, potentially causing bloody diarrhea that can progress to hemolytic uremic syndrome (HUS), a life-threatening condition with long-term implications.
Many antibiotics can stimulate the production of Shiga toxin, making infections worse and increasing the risk of HUS. They are therefore not generally recommended for infections and patients are typically only treated symptomatically.
Noting the need for strategies to eradicate STEC strains while preventing toxin release, the researchers examined the value of deploying phages—a type of virus that selectively infects and kills bacteria.
Phage-based products are already used to decontaminate food products but, as natural phages do not directly inhibit toxin production, the team investigated whether genetic engineering offered promising solution.
Galtier and colleagues engineered a delivery vector that recognized most clinical isolates from O157:H7 E. coli strains that are commonly associated with human disease, while ensuring a direct shutdown of toxin production.
Previously, the investigators had successfully used a λ phage-derived particle with engineered receptor binding proteins (RBPs) to deliver a base editor to E. coli colonizing the mouse gut.
Building on this λ-based platform, they developed EB003, a rationally engineered antimicrobial that delivers a nonreplicative CRISPR-Cas12 system programmed to target more than 99% of gene variants for stx toxins in E. coli O157 clinical isolates.
The team demonstrated that their nonreplicative CRISPR-Cas antimicrobial was efficient targeting of most clinically relevant O157 E. coli strains in vitro.
It led to a reduction of bacterial load in a mouse gut colonization model, as well as the mitigation of symptoms in an infant rabbit disease model, including reduced toxin production.
![Oral administration of the engineered CRISPR-Cas delivery particle, EB003, significantly reduces disease severity in an infant rabbit model of Shiga toxin-producing E. coli (STEC) infection. [Eligo Bioscience]](https://www.insideprecisionmedicine.com/wp-content/uploads/2026/05/Fig6_Revised-252x300.jpg)
“A key advantage of EB003 over conventional antibiotics is its ability to eliminate O157 STEC without inducing Stx release, a major limitation of current treatments such as fluoroquinolones,” they reported.
“This could translate into a safer therapeutic option, reducing the risk of HUS in patients with a STEC infection.”
The post Precision, Gene-Edited Antimicrobial Targets Difficult-to-Treat <i>E. Coli</i> appeared first on Inside Precision Medicine.
Accuracy in the Estimation of Self-Reported Knee Brace Wear Time in Young Adults With a Symptomatic Knee Following ACL Reconstruction: Secondary Analysis of a Pilot Randomized Controlled Trial
Fixed Versus Lottery Incentives for Promoting Engagement With a Cadence-Based Smartphone App: Randomized Crossover Trial
Trial Registration: UMIN Clinical Trials Registry UMIN000052303; https://tinyurl.com/ycx87a49
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Largest Rare Variant–Lipid Association Study Finds Heart Disease Targets
A landmark week for cardiovascular genetics opened with huge news from the gene-editing field: Eli Lilly’s experimental therapy VERVE-102, a single-dose PCSK9 base editor designed for patients with heterozygous familial hypercholesterolemia (FH) and premature coronary artery disease (CAD), demonstrated durable cholesterol-lowering effects in early studies. While the result marks one of the strongest signs yet that in vivo gene editing could become a practical treatment for inherited cardiovascular disease, it’s just scratching the surface of the enormous number of uncharacterized genetic variants that influence cholesterol levels and heart disease risk across global populations.
The largest rare variant association with blood lipids study ever reported may provide the roadmap to heart disease mechanistic and clinical insights. In a Nature Genetics study analyzing data from more than one million individuals, researchers identified thousands of rare coding variants linked to cholesterol and triglyceride (TG) levels, including several genes strongly associated with coronary artery disease. The findings could accelerate the development of precision medicines for dyslipidemia and improve the diagnosis of inherited lipid disorders such as familial hypercholesterolemia.
Diversity and scale
FH is caused by rare mutations that raise LDL-C, increasing the risk of early-onset CAD, a leading cause of premature death worldwide. Although statins and other lipid-lowering therapies can significantly lower cardiovascular risk, FH is underdiagnosed and undertreated. Many FH-associated variants have variable penetrance, so some carriers have severe disease and others have milder symptoms, adding to the complexity.
Accurate variant-specific risk assessment is becoming increasingly important as genetic screening expands. Most genetic databases are biased toward Europeans, making it difficult to classify disease-causing variants in non-Europeans.
To fill this gap, Satoshi Koyama, MD, PhD, led a research team across academic and medical institutions in the Boston area that analyzed exome sequencing and blood lipid data (total cholesterol, LDL-C, HDL-C, and TG) from Million Veteran Program, UK Biobank, and All of Us participants. More than 230,000 participants came from historically underrepresented populations, making this one of the most diverse large-scale lipid genetics studies conducted to date.
Mechanistic and clinical implications
Their analysis uncovered nearly three million rare coding variants, including more than 214,000 predicted loss-of-function mutations, 2.7 million missense variants, and over 23,000 cryptic splice variants that may disrupt gene processing. In total, the team evaluated over 10 million variant-phenotype associations. The results revealed 800 exome-wide significant additive associations across 184 genetic loci, along with 109 recessive associations involving 53 genes. Many of the strongest signals appeared in genes already known to regulate lipid metabolism and cardiovascular disease, including PCSK9, LDLR, APOB, NPC1L1, and APOC3.
The study also identified five lipid-associated genes significantly linked to CAD risk, highlighting potential therapeutic targets. One particularly intriguing gene was RORC, which encodes the transcription factor RORγ. Previous laboratory and animal studies suggested that suppressing RORγ improves metabolic health and reduces atherosclerosis. Consistent with those findings, the study showed that loss-of-function variants in RORC appeared protective against CAD in humans.
Another key finding involved cryptic splice variants, a class of mutations often overlooked in clinical genetics. The researchers used machine-learning-based splice prediction tools to show that these variants had biological effects similar to canonical loss-of-function mutations, suggesting that many clinically important variants may be underestimated.
The study also found that 13% of missense mutations produced hypermorphic alleles that increased gene activity, unlike most loss-of-function variants. Existing computational prediction tools frequently fail to identify these variants, potentially limiting the sensitivity of current genetic testing approaches.
Koyama and colleagues also detected strong recessive genetic effects that standard additive models may miss entirely. Because homozygous rare variants are uncommon, their contribution to disease has historically been difficult to measure. The findings suggest that recessive inheritance may explain part of the “missing heritability” in complex cardiovascular disease.
The researchers found that most rare variants exerted similar effects across populations, even when variant frequencies differed substantially between ancestries. The study identified 130 alleles observed primarily or exclusively in non-European populations, emphasizing the importance of expanding genetic research beyond European cohorts to improve equitable diagnosis and drug discovery.
From screening to saving hearts
Beyond biological discovery, the study carries important clinical implications. By comparing their findings with curated pathogenic variant databases, the investigators confirmed many established classifications while identifying variants that may warrant reclassification. Two newly highlighted variants enriched in non-European populations may represent previously underrecognized causes of familial hypercholesterolemia.
Although the research focused mainly on rare coding variants rather than noncoding DNA, the authors argue that population-scale sequencing studies can now provide clinically actionable insights into disease mechanisms, pathogenicity, penetrance, and prognosis. Together, the findings offer a powerful new resource for cardiovascular genetics at a time when therapies such as PCSK9 gene editing are beginning to move from concept to clinic.
The post Largest Rare Variant–Lipid Association Study Finds Heart Disease Targets appeared first on Inside Precision Medicine.
STAT+: Heart patch engineered from stem cells revved up weakened hearts
Hearts can’t heal themselves.
After a heart attack or other cardiovascular insult, hearts can’t regenerate weakened muscles, leaving them less able to pump blood throughout the body. While medications to manage symptoms of heart failure — including newer obesity drugs — have been improving outcomes, many people ultimately face only two solutions: a heart transplant or heart device implant.
Now a small new study reports progress with a novel method. After people received patches of heart muscle engineered from induced pluripotent stem cells, their re-muscularized heart walls thickened, revving up pumping ability and modestly improving quality of life. The biological ventricular assist tissue in a patch, called BioVAT for short, was conceived as a bridge to either transplant, where wait times are long, or to implantation of a left ventricular assist device, or LVAD, in end-stage heart failure. A larger trial will help determine who might be the best candidate for this approach and how durable it might be.

